The pulmonary toxicity of some environmental organohalogens is well established while some others are strongly suspected of having pulmonary toxicity. The objective of this research is to show that some organohalogen compounds induce lesions in the lung more readily than they do in the liver, in part, because of the relatively low aldehyde dehydehydrogenase activities in pulmonary tissues. We will show direct correlations between the biotransformation of organohalogens to aldehydes and pulmonary injury. It will also be shown that the aldehyde intermediates of many of these agents are formed in the liver, since the lung is also deficient in alcohol dehydrogenases. Changes in activities of some pulmonary enzymes will be established as biochemical indices of pulmonary injury. Trichloroethylene, halogenated ethers and 2-chloroethanol have been selected as primary compounds in this investigation because they are established environmental toxicants with widely different chemical properties. Biotransformation to aldehydes is one of the few common properties of all these agents. The relationship between biotransformation to aldehydes and pulmonary toxicity will be established by 1) Pretreatment with drugs which change the balance of active intermediates in organohalogen metabolism. 2) Studying the accumulation of aldehyde intermediates in lung and assessing the potential of these intermediates to initiate toxic reactions by covalent binding or lipid peroxidation. 3) Comparing the pulmonary toxicities to other organohalogens with similar chemical properties but are not converted to aldehydes. 4) Studying the organohalogen toxicities in animals maintained on restrictive diets, all of which are known to influence toxicity/carcinogenicity but only some of which are known to influence biotransformation.